Abstract. Chronic hepatitis B (CHB) is one of the most common types of infectious diseases worldwide. The interaction between hepatitis B virus (HBV) and the host immune response is vital for the clinical outcome of HBV infection. Costimulatory signals are key factors for the host immune response and play a critical role in innate immunity, particularly antiviral immunity. The aim of the present study was to investigate the correlation between the expression levels of costimulatory molecules and the different states of CHB infection, including the expression levels prior to and following treatment with antiviral agents. The expression levels of CD28, CTLA-4, PD-1, Tim-3 and T-cell subsets were determined by flow cytometry. The load of HBV DNA in the serum was detected by quantitative polymerase chain reaction and the serology markers, including HBeAg and alanine aminotransferase (ALT), were measured by conventional methods. Compared to the healthy control group, the expression levels of CD28 and CTLA-4 on CD4 T cells prior to and following treatment with antiviral agents (the pre-and post-treatment groups, respectively) were significantly decreased, while the expression levels of Tim-3 on CD4 and CD8 T cells were significantly increased. In addition, the expression levels of PD-1 on CD4 and CD8 T cells in the pre-treatment group were significantly increased compared to those in the post-treatment and healthy control groups. Moreover, the multivariate analysis revealed that the levels of ALT and HBV-DNA in the serum were significantly positively correlated with PD-1 expression levels. In conclusion, the expression levels of these costimulatory molecules reflect the immune dysfunction of T cells in patients with CHB and, combined with T-cell subset analysis may be used as a novel evaluation system of immune function in patients with HBV infection.
IntroductionChronic hepatitis B (CHB) is one of the most common types of infectious diseases worldwide. It was previously demonstrated that hepatitis B virus (HBV) is not directly cytopathic and that the interactions between HBV and the host immune response are crucial for the clinical outcome of HBV infection (1,2). The main cause of CHB is considered to be a cell immunity function disorder. Briefly, HBV evades the cellular immune response, avoids clearance and may cause persistent viral infections. During this process, T cells play a vital role in the immune function (3). During the process of immune response, the HBV antigens are processed by antigen-presenting cells (APCs) and presented to naïve T cells by major histocompatibility complex (MHC) molecules. Subsequently, these cells deliver a primary signal to initiate T-cell activation by engaging the T-cell receptor̸CD3 complex with foreign antigens associated with MHC molecules (4). The activation of T cells is also regulated by the balance between positive and negative signals. This balance is maintained by the interaction of costimulatory or coinhibitory receptors on T cells and their ligands on APCs. These stimul...
The relative expression of serum miR-202 in MM patients was significantly higher than that in healthy controls, and therefore it may prove to be useful in the auxiliary diagnosis of MM.
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